Pollutant gases, such as ozone and sulfur dioxide, produce mucociliary dysfunction in the airways. This mucociliary dysfunction is manifest as airway epithelial damage (including loss of cilia), reduced ciliary beating, reduced mucus transport, and secretory tissue hypeplasia. It has been suggested that pollutant-induced mucociliary dysfunction is accentuated in allergic airways, and can increase the severity of allergic airway disease. Hypersecretion of airway mucus in response to pollutants may play an important role in these pollutant-induced effects, through there is little or no evidence supporting this hypothesis. The purposes of these studies are therefore to determine; l) the effect of acute exposure to pollutants (ozone and/or sulfur dioxide on airway mucus secretion, in terms of basal secretion of mucus glycoproteins, ion fluxes, and responsiveness to antigen and known secretogogues, in allergic sheep, 2) the roles of direct actions (i.e. release of chemical mediators) and reflex neural actions in these pollutant-induced changes in airway mucus secretion, 3) the effects of chronic pollutant exposure on airway mucus secretion in normal and in allergic sheep, and to determine specifically if pollutant-induced changes are accentuated in allergic air ways, and 4) if chronic pollutant exposure of allergic sheep can increase the mucus hypersecretion in response to antigen. Mucus secretion will be assessed by measurement of the output of mucus glycoproteins (radiolabelled with 35SO4 and/or 3H-threonine) and by measurement of transtracheal fluxes of 36 Cl and 22 Na: net ion flux towared the airway lumen is an indicator of water movement into the airway, and thus of the volume of mucus secreted. Since the sheep has been established as a realistic animal model for studying allergic airway disease and pollutant-induced airway abnormailities,it is hoped that these studies will explain the mechanism and the consequences of pollutant-induced changes in airway mucus secretion in normals and in asthmatics.